Ampelopsin Improves Cognitive Impairment in Alzheimer’s Disease and Effects of Inflammatory Cytokines and Oxidative Stress in the Hippocampus

Wu, Yan; Lv, Wei; Li, Yueyang; Liu, Dandan; He, Xiuting; Liu, Ting

doi:10.2174/1567205016666191203153447

Cited by 10 publications

(6 citation statements)

References 37 publications

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“…Moreover, elevated levels of TNF-α in hippocampus have been associated with various neurological diseases such as Alzheimer's disease, depression and chronic pain [14][15][16]. Thus, in the present study, in HT22 cells, we explored the effect and possible mechanism of miR-29c on TNF-α-induced ROS production and cell apoptosis.…”

Section: Introductionmentioning

confidence: 96%

MiR-29c Inhibits TNF-α-Induced ROS Production and Apoptosis in Mouse Hippocampal HT22 Cell Line

Wang

et al. 2022

Neurochem Res

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Recent reports have suggested that abnormal miR-29c expression in hippocampus have been implicated in the pathophysiology of some nervous system disease. However, many aspects underlying mechanism of miR-29c in regulating cellular functions in hippocampal neurons are not clear. In this study, HT22 cells were infected with lentivirus containing miR-29c or miR-29c sponge. Cell counting kit-8 (CCK8) and lactate dehydrogenase (LDH) assay kit were applied to evaluate cell viability and toxicity before and after TNF-α application. The intracellular reactive oxygen species (ROS) concentration were evaluated using dihydroethidium (DHE) staining and the mitochondrial membrane potential (MMP) was determined using Tetramethylrhodamine methyl ester (TMRM) staining. Cellular apoptosis was observed via TUNEL staining assay and Hoechst 33258 staining and measured by the expression of cleaved caspase-3, -8 and − 9. The expression of miR-29c and TNFR1, Bcl-2, Bax, TRADD and FADD was analyzed by PCR or WB. As a result, we found that miR-29c overexpression signi cantly attenuated decreases in cell viability, release of LDH and apoptosis in TNF-α-treated HT22 cells. Furthermore, the high expression of miR-29c can signi cantly prevented TNF-α-induced oxidative injuries via the decrease of intracellular ROS levels and the increase of MMP. TNF-α-induced increase in Bax and cleaved-caspase-9 and the decrease of Bcl-2 was attenuated after transfection of HT22 cells with miR-29c. Moreover, over-expression of miR-29c signi cantly inhibits the increased expression of TNFR1, TRADD, FADD, cleaved caspase-8 and − 3. However, in HT22 cells transfected with miR-29c sponge, TNF-α-induced cytotoxicity and oxidative stress, as well as elevated expression of TNFR1, TRADD and FADD were exacerbated. Our ndings indicated that miR-29c overexpression attenuates TNF-α-induced HT22 cells injury through inhibiting mitochondrial oxidative stress-induced apoptosis. In addition, TNF-αinduced TNFR1 activation, FADD association and caspase 8 recruitment may be impaired by miR-29c. Therefore, miR-29c might be a potential therapeutic target for the treatment of TNF-α-induced neurotoxicity.

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Section: Introductionmentioning

confidence: 96%

MiR-29c Inhibits TNF-α-Induced ROS Production and Apoptosis in Mouse Hippocampal HT22 Cell Line

Wang

et al. 2022

Neurochem Res

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“…The activities of them in serum and organ tissues can reflect the level of antioxidants and represent the antioxidant damage ability of the body. 8-iso-PGF2α is a reliable indicator reflecting the degree of oxidative stress [ 31 , 32 ]. The level of HMGB1 is closely related to the prognosis of sepsis.…”

Section: Discussionmentioning

confidence: 99%

High Concentration Hydrogen Mitigates Sepsis-Induced Acute Lung Injury in Mice by Alleviating Mitochondrial Fission and Dysfunction

Zhao

Sun

Cui

et al. 2023

JPM

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Background: Multiple organ failure (MOF) is the main cause of early death in septic shock. Lungs are among the organs that are affected in MOF, resulting in acute lung injury. A large number of inflammatory factors and stress injury in sepsis can lead to alterations in mitochondrial dynamics. Numerous studies have confirmed that hydrogen can alleviate sepsis in the animal model. The purpose of this experiment was to explore the therapeutic effect of high concentration (67%) hydrogen on acute lung injury in septic mice and its mechanism. Methods: The moderate and severe septic models were prepared by cecal ligation and puncture. Hydrogen with different concentrations was inhaled for one hour at 1 h and 6 h after the corresponding surgery. The arterial blood gas of mice during hydrogen inhalation was monitored in real time, and the 7-day survival rate of mice with sepsis was recorded. The pathological changes of lung tissues and functions of livers and kidneys were measured. The changes of oxidation products, antioxidant enzymes and pro-inflammatory cytokines in lungs and serums were detected. Mitochondrial function was measured. Results: The inhalation of 2% or 67% hydrogen improves the 7-day survival rate and reduces acute lung injury as well as liver and kidney injury in sepsis. The therapeutic effect of 67% hydrogen inhalation on sepsis was related to increasing antioxidant enzyme activity, reducing oxidation products and pro-inflammatory cytokines in lungs and serums. Compared with the Sham group, mitochondrial dysfunction was alleviated in hydrogen groups. Conclusions: Hydrogen inhalation by high or low concentration can both significantly improve sepsis; however, a high concentration demonstrates a better protective effect. High concentration hydrogen inhalation can significantly improve the mitochondrial dynamic balance and reduce the lung injury in septic mice.

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“…NADPH oxidase (NOX) belongs to a group of electron-transporting transmembrane enzymes that contribute to ROS generation in many tissues (42) and it has been reported to be vital in the progression of neurodegenerative diseases, including AD (43). In turn, the accumulation of ROS also could upregulate NOX expression.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 alleviates lipopolysaccharide‑induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells

et al. 2021

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Lipopolysaccharide (LPS) is a toxic component of cell walls of Gram-negative bacteria that are widely present in gastrointestinal tracts. Increasing evidence showed that LPS plays important roles in the pathogeneses of neurodegenerative disorders, such as Alzheimer's disease (AD). NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. The NLRP1 inflammasome can be activated in response to an accumulation of ROS in neurons. However, it is still unknown whether LPS exposure can deteriorate neuronal damage by activating NOX2-NLRP1 inflammasomes. Ginsenoside Rg1 (Rg1) has protective effects on neurons, although whether Rg1 alleviates LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes remains unclear. In the present study, the effect of concentration gradients and different times of LPS exposure on neuronal damage was investigated in HT22 cells, and further observed the effect of Rg1 treatment on NOX2-NLPR1 inflammasome activation, ROS production and neuronal damage in LPS-treated HT22 cells. The results demonstrated that LPS exposure significantly induced NOX2-NLRP1 inflammasome activation, excessive production of ROS, and neuronal damage in HT22 cells. It was also shown that Rg1 treatment significantly decreased NOX2-NLRP1 inflammasome activation and ROS production and alleviated neuronal damage in LPS-induced HT22 cells. The present data suggested that Rg1 has protective effects on LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes in HT22 cells, and Rg1 may be a potential therapeutic approach for delaying neuronal damage in AD.

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Ampelopsin Improves Cognitive Impairment in Alzheimer’s Disease and Effects of Inflammatory Cytokines and Oxidative Stress in the Hippocampus

Cited by 10 publications

References 37 publications

MiR-29c Inhibits TNF-α-Induced ROS Production and Apoptosis in Mouse Hippocampal HT22 Cell Line

MiR-29c Inhibits TNF-α-Induced ROS Production and Apoptosis in Mouse Hippocampal HT22 Cell Line

High Concentration Hydrogen Mitigates Sepsis-Induced Acute Lung Injury in Mice by Alleviating Mitochondrial Fission and Dysfunction

Ginsenoside Rg1 alleviates lipopolysaccharide‑induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells

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